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Hyperinsulinism In Newborns

Hyperinsulinism Of The Newborn.

Hyperinsulinism Of The Newborn.

1. Semin Perinatol. 2000 Apr;24(2):150-63. (1)Department of Endocrinology and Metabolism, Hebrew University-Hadassah Medical Center, Jerusalem, Israel. [email protected] Neonatal hyperinsulinism (HI) is a clinical syndrome of pancreatic beta-celldysfunction characterized by failure to suppress insulin secretion in thepresence of hypoglycemia. Although rare, it is the most common cause forpersistent hypoglycemia in the newborn period. Treatment can be extremelydifficult, and partial pancreatectomy is frequently required to prevent recurrenthypoglycemia and irreversible brain damage. In the last 5 years much has beenlearned about the pathophysiology of this disease. In most patients, the disease is caused by recessive mutations in either of the 2 functional subunits of thebeta-cell KATP channel (SUR1 or Kir6.2). Although in most families, the diseaseis transmitted as an autosomal recessive trait, a novel form of transmission,resulting in focal involvement of the pancreas has recently been described. Notall patients with HI have mutations in the KATP channel genes. An activatingmutation in the "glucose sensor" glucokinase has recently been reported in onefamily with diazoxide-responsive autosomal dominant hyperinsulinemichypoglycemia. Also, a new syndrome of hyperinsulinism associated with benignhyperammonemia was recently described and found to be caused by activatingmutations in the glutamate dehydrogenase (GDH) gene (GLUD-1). Thus, the clinical syndrome of HI can be caused by mutations in 4 different genes and can betransmitted as either a recessive or a dominant trait. These findings aid in the therapeutic decision-making process and improve the accuracy and precision ofgenetic counseling. Despite these recent discoveries, however, the metabolicorigin of the disease Continue reading >>

Congenital Hyperinsulinism

Congenital Hyperinsulinism

General Discussion Congenital hyperinsulinism (HI) is the most frequent cause of severe, persistent hypoglycemia in newborn babies, infants, and children. In most countries it occurs in approximately 1/25,000 to 1/50,000 births. About 60% of babies with HI are diagnosed during the first month of life. An additional 30% will be diagnosed later in the first year and the remainder after that. With early treatment and aggressive prevention of hypoglycemia, brain damage can be prevented. However, brain damage can occur in children with HI if the condition is not recognized or if treatment is ineffective in the prevention of hypoglycemia. Insulin is the most important hormone for controlling the concentration of glucose in the blood. As food is eaten, blood glucose rises and the pancreas secretes insulin to keep blood glucose in the normal range. Insulin acts by driving glucose into the cells of the body. This action of insulin maintains blood glucose levels and stores glucose as glycogen in the liver. Once feeding is completed and glucose levels fall, insulin secretion is turned off, allowing the stores of glucose in glycogen to be released into the bloodstream to keep blood glucose normal. In addition, with the switching off of insulin secretion, protein and fat stores become accessible and can be used instead of glucose as sources of fuel. In this manner, whether one eats or is fasting blood glucose levels remain in the normal range and the body has access to energy at all times. This close regulation of blood glucose and insulin secretion does not occur normally in people who have HI. The beta cells in the pancreas, which are responsible for insulin secretion, are blind to the blood glucose level and secrete insulin regardless of the blood glucose concentration. As a resu Continue reading >>

Hyperinsulinism In Infancy And Childhood: When An Insulin Level Is Not Always Enough

Hyperinsulinism In Infancy And Childhood: When An Insulin Level Is Not Always Enough

Background: Hypoglycemia in infants and children can lead to seizures, developmental delay, and permanent brain damage. Hyperinsulinism (HI) is the most common cause of both transient and permanent disorders of hypoglycemia. HI is characterized by dysregulated insulin secretion, which results in persistent mild to severe hypoglycemia. The various forms of HI represent a group of clinically, genetically, and morphologically heterogeneous disorders. Content: Congenital hyperinsulinism is associated with mutations of SUR-1 and Kir6.2, glucokinase, glutamate dehydrogenase, short-chain 3-hydroxyacyl-CoA dehydrogenase, and ectopic expression on β-cell plasma membrane of SLC16A1. Hyperinsulinism can be associated with perinatal stress such as birth asphyxia, maternal toxemia, prematurity, or intrauterine growth retardation, resulting in prolonged neonatal hypoglycemia. Mimickers of hyperinsulinism include neonatal panhypopituitarism, drug-induced hypoglycemia, insulinoma, antiinsulin and insulin-receptor stimulating antibodies, Beckwith-Wiedemann Syndrome, and congenital disorders of glycosylation. Laboratory testing for hyperinsulinism may include quantification of blood glucose, plasma insulin, plasma β-hydroxybutyrate, plasma fatty acids, plasma ammonia, plasma acylcarnitine profile, and urine organic acids. Genetic testing is available through commercial laboratories for genes known to be associated with hyperinsulinism. Acute insulin response (AIR) tests are useful in phenotypic characterization. Imaging and histologic tools are also available for diagnosing and classifying hyperinsulinism. The goal of treatment in infants with hyperinsulinism is to prevent brain damage from hypoglycemia by maintaining plasma glucose levels above 700 mg/L (70 mg/dL) through pharmacologi Continue reading >>

Hyperinsulinism Center

Hyperinsulinism Center

Learning that one of the world's most respected congenital hyperinsulinism centers is right here at Cook Children's can be a life-saving moment. Congenital hyperinsulinism (CHI) is the most common cause of hypoglycemia (low blood sugar) in infants more than 3 days old, as well as children. If this rare, and often severe, genetic disorder is not treated, these children are at risk for seizures or even permanent brain damage. Finding the right care is very important in preventing irreversible damage and improving quality of life. Rare Disease Heroes. We are proud to be awarded the distinction of Rare Disease Heroes for our work in endocrinology and hyperinsulinism. This recognition is given to hospitals and clinicians that have excelled in advancing the management of rare diseases across 5 specialties: Endocrinology , Genetics , Hematology , Lysosomal Diseases , and Neurology . One of the first programs in the nation, Cook Children's Hyperinsulinism Center uses a specialized team approach to treat congenital hyperinsulinism (CHI). Hyperinsulinism (HI) affects many areas of the body, so to truly treat every aspect of HI each child is seen by top physicians, nurses, researchers and specialists in the field. These medical professionals have spent additional years of intense study and have dedicated their practice to focusing on CHI. That means your child has access to the best care available. It is this level of treatment that has helped earn our program a distinguished international reputation for extraordinary care and achieving positive results. A new surgery at Cook Children's Medical Center is offering a cure for babies born with CHI, a rare disorder of the pancreas. Why choose Cook Children's Hyperinsulinism Center? Cook Children's offers one of only 2 full-service co Continue reading >>

Hyperinsulinism | Great Ormond Street Hospital

Hyperinsulinism | Great Ormond Street Hospital

Transient hyperinsulinism can occur in infants with no predisposing factors such as those listed above. More research is needed to understand why transient hyperinsulinism occurs. Some syndromes also present in the newborn period with hyperinsulinaemic hypoglycaemia. In infants with Beckwith Weidermann syndrome, an overgrowth syndrome, up to 50 per cent have been observed to develop hyperinsulinaemic hypoglycaemia. Histologically there are two subtypes of CHI namely diffuse and focal. The diffuse type affects the whole of the pancreas whereas the focal form is confined to a tint region of the pancreas. The remaining pancreas is anatomically and functionally normal. In focal CHI, a specific area of the pancreas is affected. Focal lesions are usually small, measuring 2mm to 10mm across. Beta-cells in the focal lesion have enlarged nuclei (centre of the cell) surrounded by normal tissue. Around 40 to 50 per cent of infants with persistent CHI will have the focal form. Diffuse CHI affects the entire pancreas. It can be inherited in a recessive or dominant manner or can occur sporadically. The management of diffuse and focal disease is different. Focal disease can now be cured if the lesions are located accurately and removed completely. However, diffuse disease will require removal of almost the entire pancreas, if it does not respond to medical management. As CHI is a congenital condition, a child usually starts to show symptoms within the first few days of life, although very occasionally symptoms may appear later in infancy. Symptoms of hypoglycaemia can include floppiness, shakiness, poor feeding and sleepiness, all of which are due to the low blood glucose levels. Seizures (fits or convulsions) can also occur, again due to low blood glucose levels. If the childs blood Continue reading >>

Advances In Diagnosis And Treatment Of Hyperinsulinism In Infants And Children

Advances In Diagnosis And Treatment Of Hyperinsulinism In Infants And Children

Advances in Diagnosis and Treatment of Hyperinsulinism in Infants and Children Division of Endocrinology, Childrens Hospital of Philadelphia, Philadelphia, Pennsylvania 19104 Search for other works by this author on: The Journal of Clinical Endocrinology & Metabolism, Volume 87, Issue 11, 1 November 2002, Pages 48574859, Charles A. Stanley; Advances in Diagnosis and Treatment of Hyperinsulinism in Infants and Children, The Journal of Clinical Endocrinology & Metabolism, Volume 87, Issue 11, 1 November 2002, Pages 48574859, In infants and children, as in adults, the most common cause of persistent hypoglycemia is hyperinsulinism. However, unlike adults, hyperinsulinism in children most often represents a congenital disorder rather than an acquired islet adenoma. Many children are unresponsive to medical therapy, and near total pancreatectomy is often required because of intractable hypoglycemia. Uncontrolled hypoglycemia may lead to seizures or permanent brain damage. Developmental delay or retardation has been reported to occur in 2550% of affected children. In recent years, concepts about hyperinsulinism in infancy have evolved rapidly as reflected in the changing nomenclature for the disorder. When originally described by MacQuarrie as idiopathic hypoglycemia of infancy in 1954, insulin was not considered to be the mechanism of hypoglycemia, because insulinomas were known to be rare in infants and children. One of the first applications of the insulin RIA in the 1960s by Berson and Yallow, however, identified insulin as the underlying problem. By 1970, the disorder had become known as nesidioblastosis through studies of pancreatic pathology by Yakovak et al. ( 1 ). This term implied that hyperinsulinism was due to an anomaly in islet development in which there was a Continue reading >>

Congenital Hyperinsulinism: A Serious Yet Poorly Understood Condition

Congenital Hyperinsulinism: A Serious Yet Poorly Understood Condition

Follow all of ScienceDaily's latest research news and top science headlines ! Congenital hyperinsulinism: A serious yet poorly understood condition Diabetes is characterized by a deficiency of insulin. The opposite is the case in congenital hyperinsulinism: patients produce the hormone in excessive quantities. This leads to chronic hypoglycemia. The disorder can lead to serious brain damage and even death in the worst cases. Hyperinsulinism is linked to the GDH protein. When open (at left), the protein can more easily attach itself to a molecule that is necessary for its activity than when it is closed (at right): this sends a signal instructing the pancreas to produce insulin. A mutation of the GDH protein disrupts this mechanism and keeps the protein open, which in turn leads to insulin overproduction. Hyperinsulinism is linked to the GDH protein. When open (at left), the protein can more easily attach itself to a molecule that is necessary for its activity than when it is closed (at right): this sends a signal instructing the pancreas to produce insulin. A mutation of the GDH protein disrupts this mechanism and keeps the protein open, which in turn leads to insulin overproduction. Diabetes is characterised by a deficiency of insulin. The opposite is the case in congenital hyperinsulinism: patients produce the hormone too frequently and in excessive quantities, even if they haven't eaten any carbohydrates. Since the function of insulin is to metabolise sugars, excess production of insulin leads to chronic hypoglycaemia. The brain, which devours vast quantities of energy, is perpetually undernourished. The disorder can therefore lead to serious brain damage and even death in the worst cases. A team at the University of Geneva (UNIGE), Switzerland, supported by the Swi Continue reading >>

Neonatal Transient Idiopathic Hyperinsulinism: Case Report

Neonatal Transient Idiopathic Hyperinsulinism: Case Report

Neonatal Transient Idiopathic Hyperinsulinism: Case Radouani MA, Azzaoui S, Kabiri M and Amina *Department of Medicine and Neonatal Resuscitation, National Center for Neonatology and Nutrition, Morocco *Corresponding author: Amina Barkat, Department of Medicine and Neonatal Resuscitation, National Center for Neonatology and Nutrition, Childrens Hospital, Ibn Sina hospital, Ibn Rushd bd, 10100 Souissi, Rabat, Morocco, Tel: 0661385108; Email: Received: November 7, 2014 | Published: March 12, 2015 The hyperinsulinism (HI) is a common cause of hypoglycemia in the newborn. Inappropriate insulin secretion by pancreatic beta cells is responsible for severe hypoglycaemia with a high risk of brain damage. It is usually found in hypotrophic newborns and in newborns of diabetic mothers by hyperinsulinemia or secondary to an increase in anti-stress hormones. Syndromic HIs are responsible for permanent hypoglycemia. The diagnosis of idiopathic HI can be done by high insulin and C-peptide in the blood with normal pancreatic and brain imaging and a negative balance metabolic and genetic levels. We report a case of a newborn who has severe idiopathic transient hypoglycemia. This newborn male was two days old admitted for dehydration with hypoglycemia. The mother is 32 years old, primiparous blood type A positive. The pregnancy was without vaginal with immediate cry. Birth weight is 2700g. Clinical examination showed, weight W = 2500g, size S = 47cm, head circumference HC 34 cm, temperature T = 37 , heart rate HR = 160 b / m, Blood pressure BP = 55/30, blood glucose capillary GC: 0.13 g / l. The patient is polypneic, hypotonic with a fold dehydration and sunken eyes. The review noted no facial dysmorphia or micropenis and no hepatomegaly. The remainder The newborn had received a saline Continue reading >>

Congenital Hyperinsulinism

Congenital Hyperinsulinism

Topics covered include the following: Congenital Hyperinsulinism Congenital hyperinsulinism (HI) is the most frequent cause of severe, persistent hypoglycemia in newborn babies and children. In most countries it occurs in approximately 1/25,000 to 1/50,000 births. About 60% of babies with HI develop hypoglycemia during the first month of life. An additional 30% will be diagnosed later in the first year and the remainder after that. With early treatment and aggressive prevention of hypoglycemia, brain damage can be prevented. However, brain damage can occur in children with HI if their condition is not recognized or if treatment is ineffective in the prevention of hypoglycemia. The material below explains the different forms of HI, the mechanisms of each type of HI, the genetic defects responsible for HI and their mode of inheritance. There is also information on treatment options and recent advances in diagnosis. Mechanisms of Disease Insulin is the most important hormone for controlling the concentration of glucose in the blood. As food is eaten, blood glucose rises and the pancreas secretes insulin to keep the blood glucose in the normal range. Insulin acts by driving glucose into the cells of the body. This action of insulin has two effects 1) maintaining blood glucose levels and 2) storing glucose particularly as glycogen in the liver. Once feeding is completed and the glucose levels fall, insulin secretion is turned off, allowing the stores of glucose in glycogen to be released into the bloodstream to keep blood glucose normal. In addition, with the switching off of insulin secretion, protein and fat stores become accessible and can be used instead of glucose as sources of fuel. In this manner, whether one eats or is fasting blood glucose levels remain in the norma Continue reading >>

Effects Of Hyperinsulinism On Newborns - Medicine Bibliographies - In Harvard Style

Effects Of Hyperinsulinism On Newborns - Medicine Bibliographies - In Harvard Style

Not logged in. Log in or create an account These are the sources and citations used to research effects of hyperinsulinism on newborns. This bibliography was generated on Cite This For Me on Insulin assays and reference values - EM|consulte Your Bibliography: Em-consulte.com. (2015). Insulin assays and reference values - EM|consulte. [online] Available at: [Accessed 7 Dec. 2015]. Cortisol in saliva--reference ranges and relation to cortisol in serum. - PubMed - NCBI Your Bibliography: AC, A. (2015). Cortisol in saliva--reference ranges and relation to cortisol in serum. - PubMed - NCBI. [online] Ncbi.nlm.nih.gov. Available at: [Accessed 7 Dec. 2015]. Mosby's Manual of Diagnostic and Laboratory Tests, 4th edition Your Bibliography: Pagana and Pagana. (n.d.). Mosby's Manual of Diagnostic and Laboratory Tests, 4th edition. Your Bibliography: Luxton, R. (2008). clinical biochemistry. 2nd ed. oxfordshire, pp.72-74,117-121. Pancreatic -cell KATP channels: Hypoglycaemia and hyperglycaemia In-text: (Bennett, James and Hussain, 2010) Your Bibliography: Bennett, K., James, C. and Hussain, K. (2010). Pancreatic -cell KATP channels: Hypoglycaemia and hyperglycaemia. Rev Endocr Metab Disord, 11(3), pp.157-163. Edghill, E. L., Flanagan, S. E. and Ellard, S. Permanent neonatal diabetes due to activating mutations in ABCC8 and KCNJ11 In-text: (Edghill, Flanagan and Ellard, 2010) Your Bibliography: Edghill, E., Flanagan, S. and Ellard, S. (2010). Permanent neonatal diabetes due to activating mutations in ABCC8 and KCNJ11. Rev Endocr Metab Disord, 11(3), pp.193-198. Your Bibliography: Medicinehack.com. (2011). August 2011 ~ Medicine Hack. [online] Available at: [Accessed 9 Dec. 2015]. Insulin secretion from beta cells within intact islets: Location matters Your Bibliography: Hoang Do, O Continue reading >>

[full Text] Managing Congenital Hyperinsulinism: Improving Outcomes With A Multidi | Rred

[full Text] Managing Congenital Hyperinsulinism: Improving Outcomes With A Multidi | Rred

Division of Endocrinology and Diabetes, The Childrens Hospital of Philadelphia, Philadelphia, PA, USA Abstract: Congenital hyperinsulinism (CHI) is the most common cause of persistent hypoglycemia in pediatric patients and is associated with significant risk of hypoglycemic seizures and developmental delays. CHI results from mutations in at least nine genes that play a role in regulating beta-cell insulin secretion. Thus, patients with CHI have dysregulated insulin secretion that is unresponsive to blood glucose level. Each different genetic etiology of CHI is associated with particular clinical characteristics that affect management decisions. Given the broad phenotypic spectrum and relatively rare prevalence of CHI, it is important that patients with CHI be evaluated by clinicians experienced with CHI and the multiple subspecialty services that are necessary for the management of the disorder. In this review, we summarize the pathophysiology and genetic causes of CHI and then focus primarily on the most common genetic cause (mutations in the ATP-gated potassium [KATP] channel) for further discussion of diagnosis, medical and surgical management, and potential acute and chronic complications. We provide insight from relevant published studies and reports, in addition to anecdotal information from our centers clinical experience in caring for over 400 patients with CHI. Careful assessment of each patients individual pathophysiology is necessary to determine the appropriate treatment regimen, and continued close follow-up and monitoring of disease- and treatment-related complications are essential. Although significant improvements have been made in the past several years with regard to diagnosis and management, given the continued high morbidity rate in patients with C Continue reading >>

Persistent Hyperinsulinemic Hypogylcemia In Infants

Persistent Hyperinsulinemic Hypogylcemia In Infants

Persistent Hyperinsulinemic Hypogylcemia in Infants Persistent hyperinsulinemic hypoglycemia of infancy (PHHI) is the most common cause of recurrent hypoglycemia in neonates and infants. It is a disorder of glucose homeostasis characterized by unregulated hyperinsulinemia and profound hypoglycemia. PHHI may be differentiated from other causes of hypoglycemia by demonstrating the persistence of inappropriately high insulin levels regardless of blood glucose concentration. Prompt recognition and treatment of PHHI is critical because uncorrected hypoglycemia in the newborn period is associated with permanent damage to the central nervous system and subsequent mental retardation. The aim of therapy is to maintain euglycemia to protect the developing brain from possible damage. Despite recent advances in medical treatment, subtotal pancreatectomy is often necessary. This article will review the function of insulin, glucagon, and somatostatin, pathophysiology of hyperinsulinism, clinical manifestations, differential diagnosis, management, and reported neurologic outcomes of newborns and infants with PHHI. Persistent hyperinsulinism is a genetically heterogeneous condition associated with excessive insulin production and, although rare, it is the most common cause of severe, persistent hypoglycemia beyond the immediate neonatal period.[ 1 , 2 , 3 ] It is referred to as persistent hyperinsulinemic hypoglycemia of infancy (PHHI). PHHI was first described more than 40 years ago by McQuarrie[ 4 ] and usually presents between birth and the first 3 months of life.[ 1 , 2 ] In a noninbred White population, the estimated frequency is 1 in 50,000 live births[ 5 , 6 ] but in certain populations, such as Saudi Arabia, where approximately 50% of births occur to parents who are first or s Continue reading >>

Neonatal Hypoglycemia

Neonatal Hypoglycemia

OBJECTIVES After completing this article, readers should be able to: Describe the most common cause of prolonged neonatal hypoglycemia. List the signs of hypoglycemia. Describe the condition that has been implicated as a mechanism of hypoglycemic brain injury. Case Study A term male infant was born after an uneventful pregnancy to a 28-year-old gravida I woman who had no evidence of hyperglycemia and no chronic diseases. The infant had Apgar scores of 7 and 9 at 1 and 5 minutes, respectively. His growth parameters were in the normal range, with weight at the 60th percentile, head circumference at the 50th percentile, and length at the 50th percentile. The baby was taken to the well baby nursery, examined and bathed, and then taken to the mother for nursing at about 2 hours of age. He appeared slightly jittery at that time and was not very interested in nursing or very aware. A blood glucose concentration of 1.39 mmol/L (25 mg/dL) was obtained using a One Touch® instrument. The baby was fed 25 mL of 5% dextrose in water. The blood glucose concentration obtained 1 hour later was 2.22 mmol/L (40 mg/dL), and the baby nursed for about 5 minutes at each breast with apparent satisfaction. Jitteriness and“ lack of interest” were improved. Normal nursery routine was followed, with no comment in the chart by the nursing staff about the infant’s feeding or behavior until the second day of life when he again appeared jittery and fussy. Glucose concentration at that time was 1.11 mmol/L (20 mg/dL). The infant was fed by breast or bottle (routine 20 kcal/oz house formula) alternating every 2 hours, and clinical signs improved. One Touch® glucose concentrations obtained over the next 24 hours were variable, but overall the concentration increased, with a predischarge, preprand Continue reading >>

Orphanet: Congenital Isolated Hyperinsulinism

Orphanet: Congenital Isolated Hyperinsulinism

Prevalence is estimated at 1/50,000 live births, but it may be as high as 1/2,500 in communities with substantial consanguinity. CHI onset varies from birth through early adulthood. Neonatal onset is the most frequent; newborns, often macrosomic present with poor feeding, intolerance to fasting and persistent hypoglycemia. Hypoglycemic episodes range from mild (lethargy, hypotonia and irritability) to severe and potentially fatal episodes (apnea, seizures or coma) that lead to neurologic sequelae. In late onset CHI, patients generally present with features of hypoglycemia (pallor, profuse sweating and tachycardia). In some forms hypoglycemia may be triggered by anaerobic exercise (exercise-induced hyperinsulinism) or protein rich meals (hyperinsulinism-hyperammonemia syndrome and hyperinsulinism due to 3-hydroxylacyl-CoA dehydrogenase deficiency, see these terms). Nine genes are associated to CHI among which mutations in the genes encoding the ATP-sensitive potassium channel in pancreatic beta cells (ABCC8, KCNJ11) represent the most common defect. Persistent hypoglycemic episodes (that require intravenous glucose infusion rates of >8 mg/kg/min to maintain normoglycemia) and responsiveness to glucagon are highly indicative of CHI. Detectable serum insulin/C-peptide, low ketone bodies, suppressed fatty acids and suppressed branch chain-amino acids during hypoglycemic episodes (glycemia of <3 mmol/l) all indicate CHI. Later onset CHI may require provocative testing (e.g. oral glucose or leucine loading; formal exercise testing). Cases unresponsive to diazoxide should be classified in to focal and diffuse HI by genetic testing for (ABCC8/ KCNJ11mutations and imaging, particularly DOPA-Positron emission tomography (PET). Differential diagnosis includes transient hyperinsul Continue reading >>

Hyperinsulinism In A Neonate

Hyperinsulinism In A Neonate

Senior Clinician Educator, Pritzker School of Medicine, University of Chicago, and Department of Pediatrics, NorthShore University Health System Assistant Professor of Pediatrics and Medicine, Section of Adult and Pediatric Endocrinology, Diabetes and Metabolism, Pritzker School of Medicine, University of Chicago The publisher's final edited version of this article is available at Pediatr Ann A male patient was born small for gestational age (SGA) at 33 weeks with a birth weight of 1,663 grams (< 10th percentile) and length 43 cm (10th percentile) to a 38-year-old G5P4 mother by cesarean section due to non-reassuring fetal heart tones. Prior to delivery, his mother experienced decreased fetal movement and decelerations. At birth, he was initially well-appearing and vigorous, with Apgar scores of 7 and 8 at 1 and 5 minutes, respectively. The physical examination was unremarkable no skin findings, no facial anomalies, good tone, and the anterior fontanelle was soft and flat. The placenta, although noted to be healthy in appearance on prenatal ultrasounds, was atrophic and calcified by gross examination. The patient developed respiratory distress 1 hour after birth and was found to have a blood glucose level of 24 mg/dL. Following an intravenous (IV) bolus of 10% dextrose in water (D10W) of 2 mL/kg, his glucose was 20 mg/dL. He was started on IV fluids with a glucose infusion rate (GIR) of 7.3 mg/kg/minute, with a subsequent rise in blood glucose to 46 mg/dL. Due to prematurity, respiratory distress, and persistent hypoglycemia, a diagnostic evaluation was initiated for possible sepsis, including a complete blood count with differential and platelet count and blood cultures. The patient was started empirically on IV ampicillin and gentamicin. The patient was subsequently Continue reading >>

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